Cited by 258Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsInflammasome and immune disorders

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Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders

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Von Bernhardi, Rommy, Tichauer, Juan E., Eugenín, Jaime·2010·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2009.06537.x

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Abstract

J. Neurochem. (2010) 112, 1099–1114. Among multiple structural and functional brain changes, aging is accompanied by an increase of inflammatory signaling in the nervous system as well as a dysfunction of the immune system elsewhere. Although the long‐held view that aging involves neurocognitive impairment is now dismissed, aging is a major risk factor for neurodegenerative diseases such as Alzheimer`s disease, Parkinson`s disease and Huntington’s disease, among others. There are many age‐related changes affecting the brain, contributing both to certain declining in function and increased frailty, which could singly and collectively affect neuronal viability and vulnerability. Among those changes, both inflammatory responses in aged brains and the altered regulation of toll like receptors, which appears to be relevant for understanding susceptibility to neurodegenerative processes, are linked to pathogenic mechanisms of several diseases. Here, we review how aging and pro‐inflammatory environment could modulate microglial phenotype and its reactivity and contribute to the genesis of neurodegenerative processes. Data support our idea that age‐related microglial cell changes, by inducing cytotoxicity in contrast to neuroprotection, could contribute to the onset of neurodegenerative changes. This view can have important implications for the development of new therapeutic approaches.

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Von Bernhardi R., 2009, Immunotherapy in Alzheimer Disease: where do we stand? Where should we go?, J. Alzheimer Dis.
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Authors: Von Bernhardi, R., Tichauer, J. E., & Eugenín, J.
Affiliations: Pontificia Universidad Católica de Chile (CL)
Universidad de Santiago de Chile (CL)
ORCID: Tichauer, Juan E.
Eugenín, Jaime
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2010-02-02
Volume: 112
Issue: 5
Pages: 1099-1114
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/j.1471-4159.2009.06537.x
OpenAlex: W2027368264
Cited by: 258
References: 203
Citations by year: 2026: 2 · 2025: 11 · 2024: 16 · 2023: 14 · 2022: 13 · 2021: 21 · 2020: 20 · 2019: 19 · 2018: 18 · 2017: 13 · 2016: 15 · 2015: 16 · 2014: 10 · 2013: 22 · 2012: 23
FWCI: 1.24
Type: journal article
Language: en
Open access: green
americanae.aecid.es
Licence: other-oa
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Americanae (AECID Library) (submittedVersion, other-oa)
LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords: microglia, brain aging, neuroinflammation, neurodegenerative diseases, Toll-like receptors, microglial phenotype, Alzheimer's disease, Parkinson's disease, Huntington's disease, neuroprotection, cytotoxicity, neurodegeneration
MeSH terms: Aging, Animals, Brain, Disease Models, Animal, Humans, Iron, Gene Expression, Cytokines, Microglia, Oxidative Stress, Neurodegenerative Diseases

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Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders

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